Bacteria may only be simple single cells but many still live highly social lives. As with any busy social life, communication systems are vital for organizing a group. Bacteria communicate via chemical signalling systems collectively referred to as quorum sensing. In a new study published in BMC Systems Biology, Volkhard Helms from the Center for Bioinformatics at Saarland University, Germany and colleagues describe a computational model of the dynamic quorum sensing system of the opportunistic bacterium Pseudomonas aeruginosa.

P. aeruginosa typically infects immunocompromised patients, using its quorum sensing system to regulate several important processes during infection. This includes the formation of biofilms – communities of microorganisms that adhere to and cover surfaces – and the production of virulence factor molecules that are responsible for many of the symptoms of infection. These functions make quorum sensing systems a promising target for anti-bacterial drugs that could disrupt these lines of communication. It has also been suggested that such drugs may have the advantage over current antibiotics in being less likely to induce drug resistance.

Helms and colleagues use computational modelling to explore what effects inhibitors of various parts of the quorum sensing system would have on the bacteria P. aeruginosa.

Quorum sensing in P. aeruginosa consists of three interconnected systems, organized in a hierarchy. As many of the details of the connections remain unknown the authors use a simplified, rule-based model of these networks to determine the production of molecules used for signalling between cells and virulence factors.

Tests of the model show that despite its relative simplicity it accurately replicates behaviors of the system reported in the literature. However their findings do suggest that the topology of the molecular network as it is currently understood may need to be revised in order to accurately describe the production of virulence factors.

From this model they show that it is possible to test the effects of mutations or inhibitors that affect various components of the molecular networks. The authors find that blocking the synthesis of signalling molecules is most effective in reducing the production of these networks, and that targeting the receptor molecules is key to reducing virulence factors.